Mammalian Genome 13, 169-172 (2002). DOI: 10.1007/s00335-001-2123-x Mammalian P41OIlle Incorporating ~louse Genome 9 Springer-Verlag New York Inc. 2002 Early embryonic lethality in mice deficient in the pll013 catalytic subunit of PI 3-kinase Lei Bi, Ichiro Okabe, David J. Bernard, Robert L. Nussbaum Genetic Diseases Research Branch, National Human Genome Research Institute, National Institutes of Health, 49 Convent Drive, 4A72, Bethesda, Maryland 20892-4472, USA Received: 27 August 2001 / Accepted: 31 October 2001 An important class of phosphorylated phosphoinositides carrying a of Pik3ca die in utero between E9.5 to El0.5 because of a prolif- phosphate group at the 3' position of the inositol ring are generated erative defect (Bi et al. 1999). This result implies that other iso- by phosphoinositide 3-kinases (PI 3-kinases) which convert forms including 13 cannot compensate for the function of the PtdIns, PtdIns(4)P, and PtdIns(4,5)P 2 to PtdIns(3)P, PtdIns(3,4)P2, isoform at this stage. Here we report the successful targeting of the and PtdIns(3,4,5)P 3 respectively (Frnman et al. 1998; Vanhaese- Pik3cb encoding the beta isoform of pll0, to create a partial broeck et al. 2001). The PI 3-kinases can be grouped into three deletion allele which, in the homozygous state, leads to very early classes according
Mammalian Genome – Springer Journals
Published: Jul 31, 2007
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